Acute peripheral facial nerve palsy (FNP) is a well-described cranial nerve dysfunction of the seventh cranial nerve. The facial nerve carries motor fibres to the facial musculature, efferent secretory fibres to the lacrimal and salivary glands as well as afferent sensory fibres from the anterior two-thirds of the tongue and the external auditory canal. The onset of FNP is normally acute and causes inability to control facial muscles on the affected side. The annual incidence of FNP in children has been reported from 5 to 21 per 100 000 children/year 1-5 with up to 43/100 000 among children under 6 years of age. 4 Differential diagnosis for acquired FNP is infections (ie Lyme borreliosis/neuroborreliosis, members of the herpesvirus family and enteroviruses), trauma, tumours, leukaemia, vascular diseases, iatrogenic causes and idiopathic facial palsy (IFP) (FNP of unknown cause despite appropriate diagnostic measures). Neuroborreliosis, a tick-borne infection, is the most common identifiable cause among children and is significantly more common in children than adults. 1,4,6 In Borrelia high-endemic areas, neuroborreliosis has been reported as the cause in 23%-65% of children with FNP. 1-4,7 Whereas FNP attributable to infections is more prevalent in children, the majority of FNP among adults is IFP. The incidence of IFP increases with age as shown in a UK study where the lowest incidence was among children 0-6 years of age; 6.6 per 100 000 person years, compared to 20.1 per 100 000 years among those 15-29 years of age. 8 Larger cohorts in adults have shown a yearly incidence of IFP around 30 per 100 000. 9